The crisis facing printed medical literature. Acid paper

Medicine strives to preserve the achievements of the past for the benefit of future clinicians and scientists. However, the paper on which medical journals are printed is steadily and irreversibly decaying. Since the late 1800s, most medical journals have been published on paper prepared with acids. In recent years, publishers, authors, and archivists have become aware of the destructive effects of acid decay on medical journals. Though the cause of deterioration is well understood, the choice of a remedy is still controversial. Remedies include acid-free paper, computerization, deacidification, and microfilm. These techniques are reviewed for their reliability, comprehensiveness, and cost-effectiveness. Microfilm is recommended above other techniques as the most immediately promising solution. The authors propose that publishers be required by law to submit archival quality microfilm as a condition for copyright protection.     

Bündelhaar-Follikulitis

Zusammenfassung Bei der Bündelhaar-Follikulitis (tufted hair folliculitis) handelt es sich um eine durch Staphylococcus aureus verursachte, chronisch entzündliche und vernarbende Haarbodenerkrankung, die charakterisiert ist durch das umschriebene Auftreten von Bündelhaaren. Histopathologisch findet sich eine perifollikul?re Entzündung im oberen Bereich der Haarfollikel unter Aussparung der tiefen Follikelanteile. Innerhalb der Entzündungsareale münden mehrere Haare aus getrennten Haarwurzeln in ein gemeinsames Infundibulum mit dilatiertem Ostium. Das Krankheitsbild ist als eine Erscheinungsform der Folliculitis decalvans capillitii Quinquaud anzusehen, bei der die Auffassung besteht, da? die Infektion mit Staphylococcus aureus den pathogenetischen Initialfaktor darstellt, und Besonderheiten der Follikelanatomie und Immunantwort die individuelle Morphologie bestimmen: Dabei ist anzunehmen, da? die Ausbildung fl?chig atropher Narben mit vollst?ndigem Untergang der Hautanhangsgebilde (im Falle der Folliculitis decalvans) oder das Auftreten von Haarbündeln (im Falle der Bündelhaar-Follikulitis) von der Tiefe und dem Destruktions-Potential des Entzündungsinfiltrates abh?ngen. Die Behandlung der Bündelhaar-Follikulitis ist nicht ganz unproblematisch: Die prolongierte und wiederholte Gabe staphylokokken-wiksamer Antibiotika vermag den Krankheitsverlauf zu stabilisieren. Bereits vorhandene Haarbündel mit einer besonders hohen Rezidivneigung sollten aber – wie im vorgestellten Fall – nach M?glichkeit chirurgisch exzidiert werden.

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Summary A case of tufted hair folliculutis presenting as circumscribed, tender and inflamed areas in the occiput with residual tufted follicles in a 28-year old man is reported. Tufted hair folliculitis is a characteristic localized scarring bacterial folliculitis of the scalp due to Staphylococcus aureus. Histopathological studies reveal perifollicular inflammation around the upper portions of the follicles sparing the hair root level. Within areas of inflammation, several follicles converge toward a common follicular duct with a widely dilated opening. Currently, tufted hair folliculitis is considered a variant of folliculitis decalvans of Quinquaud. Staphylococcal infection is believed to be an initial causative factor, and underlying differences in follicular anatomy or host response may be important in determining which reaction pattern occurs in an affected individual. The development of atrophy with loss of adnexal structures (in folliculitis decalvans) or of hair tufts (in tufting folliculitis) may depend upon the depth and destructive potential of the inflammatory process. The therapeutic approach is problematic; prolonged treatment with oral antibiotics may stabilize the disease, but good and at times more definitive results (as in the presented case) have been reported after radical surgical excision of the involved areas.

Eingegangen am 2. April 1996 Angenommen am 7. Juni 1996     

Altered Excitability of the Motor Cortex after Minor Head Injury Revealed by Transcranial Magnetic Stimulation

Summary This study attempts to find out whether the motor evoked potential (MEP) elicited by single pulse and slow-rate (1 Hz) repetitive transcranial magnetic stimulation (TMS) can disclose concealed subclinical impairments in the cerebral motor system of patients with minor head injury. The motor response to single pulse TMS (STMS) of the patient groups was characterized by significantly higher threshold compared with that of the control group. The central motor conduction time, as well as the peripheral conduction time were normal in all patients pointing to cortical impairment. Two main patterns of MEP changes in response to repetitive TMS (RTMS) were observed in the patient group. A. – progressive decrease of the MEP amplitude throughout the stimulation session to a near complete abolition. B. – irregularity of the amplitude and the waveform of the MEP in a chaotic form. The MEP latency remained stable during the whole stimulation session. The MEP abnormalities recovered gradually over the period of a few months. The higher threshold of the motor response to STMS and the abnormal patterns of the MEP to RTMS seem to reflect transient impairment of cortical excitability or “cortical fatigue” in patients who sustained minor head injures. Further study is needed to evaluated the extent and the pathophysiological mechanisms of the central nervous system fatigue phenomenon following head injury.     

Androgen receptor YAC transgenic mice carrying CAG 45 alleles show trinucleotide repeat instability

X-linked spinal and bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion in the first exon of the androgen receptor (AR) gene. Disease-associated alleles (37-66 CAGs) change in length when transmitted from parents to offspring, with a significantly greater tendency to shift size when inherited paternally. As transgenic mice carrying human AR cDNAs with 45 and 66 CAG repeats do not display repeat instability, we attempted to model trinucleotide repeat instability by generating transgenic mice with yeast artificial chromosomes (YACs) carrying AR CAG repeat expansions in their genomic context. Studies of independent lines of AR YAC transgenic mice with CAG 45 alleles reveal intergenerational instability at an overall rate of approximately 10%. We also find that the 45 CAG repeat tracts are significantly more unstable with maternal transmission and as the transmitting mother ages. Of all the CAG/CTG repeat transgenic mice produced to date the AR YAC CAG 45 mice are unstable with the smallest trinucleotide repeat mutations, suggesting that the length threshold for repeat instability in the mouse may be lowered by including the appropriate flanking human DNA sequences. By sequence-tagged site content analysis and long range mapping we determined that one unstable transgenic line has integrated an approximately 70 kb segment of the AR locus due to fragmentation of the AR YAC. Identification of the cis - acting elements that permit CAG tract instability and the trans -acting factors that modulate repeat instability in the AR YAC CAG 45 mice may provide insights into the molecular basis of trinucleotide repeat instability in humans.      

A controlled trial comparing foscarnet with vidarabine for acyclovir-resistant mucocutaneous herpes simplex in the acquired immunodeficiency syndrome. The AIDS Clinical Trials Group.

BACKGROUND AND METHODS. Most strains of herpes simplex virus that are resistant to acyclovir are susceptible in vitro to both foscarnet and vidarabine. We conducted a randomized trial to compare foscarnet with vidarabine in 14 patients with the acquired immunodeficiency syndrome (AIDS) and mucocutaneous herpetic lesions that had been unresponsive to intravenous therapy with acyclovir for a minimum of 10 days. The patients were randomly assigned to receive either foscarnet (40 mg per kilogram of body weight intravenously every 8 hours) or vidarabine (15 mg per kilogram per day intravenously) for 10 to 42 days. In the isolates of herpes simplex virus we documented in vitro resistance to acyclovir and susceptibility to foscarnet and vidarabine. RESULTS. The lesions in all eight patients assigned to foscarnet healed completely after 10 to 24 days of therapy. In contrast, vidarabine was discontinued because of failure in all six patients assigned to receive it. The time to complete healing (P = 0.01), time to 50 percent reductions in the size of the lesions (P = 0.01) and the pain score (P = 0.004), and time to the end of viral shedding (P = 0.006) were all significantly shorter in the patients assigned to foscarnet. Three patients had new neurologic abnormalities while receiving vidarabine. No patient discontinued foscarnet because of toxicity. Although initial recurrences of herpes simplex infection after the index lesion had healed tended to be susceptible to acyclovir, acyclovir-resistant infection eventually recurred in every healed patient, a median of 42.5 days (range, 14 to 191) after foscarnet was discontinued. CONCLUSIONS. For the treatment of acyclovir-resistant herpes simplex infection in patients with AIDS, foscarnet has superior efficacy and less frequent serious toxicity than vidarabine. Once the treatment is stopped, however; there is a high frequency of relapse.